This work has the long-term goal of understanding myopia in the context of the biological processes by which the growth of the eye is controlled. It seems reasonable to view myopia not as a disease state, but as a defect in the process by which the eye grows toward being emmetropic (that is, neither myopic nor hyperopic). The proposal seeks to determine at what levels the control over the growth of the young eye is exerted. Specifically, we find that there is a retinal level of control, manifested by visual deprivation of a part of the retina causing the growth of the sclera only in the deprived region, apparently without the participation of the brain. We propose to study this by raising birds with one region of the retina deprived of form vision and comparing the refractive status and size of the deprived region with the visually experienced region. Then we will do the same in animals with the optic nerve severed. Preliminary indications are that visual deprivation can still produce a local myopic region even under these conditions. If simple form deprivation causes severe myopia, it may be the case that the simple chaotic visual stimulation of a strobe light can prevent myopia from developing. We propose to test this in several species. We suspect that it is not the case that all control of the growth of the eye comes from within; we plan to assess the role of the brain in experimental myopia by making lesions in the Edinger-Westphal nucleus as well as by cutting the optic nerve. We also plan to study the process by which some eyes, such as those of chicks, can recover from myopia, whereas others cannot. We wish to explore the possibility that the same internal factors that determine an individual's susceptibility to myopia also determine its ability to recover from the myopia.